Sunday 16 October 2011

The Cardiology Clinic

17 years old malay lady was referred to the cardio clinic for valve replacement therapy. She is a known case of .

In the social history, she just finished her SPM and is just staying at home with her parents. Her father is a fisherman and mother is a housewife
Admitted in July 2011 for:
1) B-Thallasemia Intermediate
　
　
2) Congenital Heart Disease in failure complicated by ventilator assisted pneumonia, sacral sore and pneumothorax
ECHO (July 2011): Thickened valve leaflets, mod AR and severe MR with valve prolapse
Tracheal Aspirate (7/7/2011): Burkhodelia cepasia
rpt culture @ 11/7/2011: burkhedellia cepasia
rpted culture on 14/7/2011: <RSA
latest TA @ 18/7/2011: no pathogen isolated
　
　
3) Right foot drop ? secondary to malpositioning whilst intubated
doing physiotherapy under rehab HSB
　
　
　
　
pt was admitted to Hospital Tanjung Karang initially for anemia
she was transfused at least 4p PC - she was told that she had thallasemia and the other family members need to be screened for it
　
　
she also complained of cough, fever, SOB and generalised edema
later on, she was transferred to HSB in view of worseining anarsace (generalised edema) where she was intubated for more than 1mth --> initially intubated then put on tracheostomy
She was treated with frusemide as inpatient
　
　
She was discharged well on T captopril 25mg BD, T metoprolol 25mg BD and hemetinics.
Currently she denied any SOB, palpitation or leg swelling
She claim to have on and off chest pain - can be at rest or on exertion
　
　
BO/ PU as normal
no diarrhea/ vomitting
no fever/ fits/ faints
　
　
　
　
　
Social & Occupational History
mother and father - not govn servants, father is a fisherman
4/8 siblings
born SVD at term - was well till age 11 years old
She presented at 11 years old with rapid breathing --> was seen in Hospital Tanjung Karang then transferred to Hosp Klang --> sb IJN for heart problem - was told that it was too early for a valve replacement therapy
　
　
3rd child - bowel operation on D2 of birth ? intussusception, currently well
no FHx of congenital heart disease
Physical ExaminationGeneral Examination
　
alert
mild pallor
small build
finger clubbing+
walking with a limp - pt not wearing her splint for the right foot drop
　
　
　
　
BP 123/ 78
HR 88bpm reg
Collapsing pulse +
no radio - radial or radio-femoral delay
JVP not raised
no stigmata of IE
　
　
Lungs: clear, no crepitations
CVS: Thrills palpable over the precordium, Apex displaced at 6th ICSMCL
HS I + II + PSM heard loudest at the LSE, radiating to the axilla
Right foot drop with reduced sensation up to right ankle
　
　
[amended >>]ECG: SR noa cute ischemic changes[<< amended]　
　
Plan: (s/b Dr Zaidi)
to rpt ECHO at Sg Buloh UiTM today
TCA Cardio x1/12
cont captopril and metoprolol - already have a one months supply
TCA nearest hospital if condition worsen
　
　
Zahirah

70 years old lady
　
　
kc
HPT
DM
non smoker, no alcohol
FHx:
3/4 siblings
all brothers and sisters have DM/ HPT
one brother died from CCF
father - has DM/ HPT/ IHD/ CVA
mother - no known medical illness
　
　
Medications: No allergies
Aspirin 150mg OD
Plavix 75mg OD
Frisemide 20mg OD
Glicazide 40mg BD
Metformin 1g BD
Isosorbide dinitrate 10mg TDS
Simvastatin 20mg ON
Trimetazidine 2mg TDS
　
　
referred from HSB for angiogram
　
　
Admitted to HSB on 27/9/2011 for Unstable angina
presented with sudden onset of heavybess oveer the central chest at rest a/w giddiness and sweating
　
　
blood Ix at HSB:
FBC - wcc 9 hb 13.6 plt 307
RP: Ur 4.6 Na 138 K 4.2 Cr 49
FBS: 7.2
Hba1c 10.6%
TFT - T415 TSH 1.03
TG 1.31
LDL 3
HDL 1.16
Tot chol 4.78
　
　
Hep Bs Ag non reactive
Hep CV Ab non reactive
HIV non reactive
　
　
ECHO @ 29/9/2011:
Chambers size: normal sizes
LV contraction: Bradycardia
Valve morphology: mild tricuspid regurgitation with PASP 22mmhg
LVH/ ASH/ SAM: LVH 1.6cm
Conclusion: EF 56%
　
　
Since discharged from HSB, no more chest pain/ SOB/ leg swelling
c/o neck pain under physio for ? cervical spondylosis
　
　
OE:
alert
pink
not tachypneic
Lungs: clear
CVS: HS I + II + no added sounds
no pedal edema
　
　
ECG - SR, T inv I, aVL, V2 - V6
　
　
Plan: (s/b Dr Zubin)
for angiogram on 1/11/2011 - pt agreeable
for GSH
keep NBM after light breakfast @ 6am
withold OHA prior to angiogram - pt informed
consent form signed
TCA cardio clinic after angiogram
　
　
Zahirah
　Cardio clinic check list:
1) Explore and address the pt's general complaints
2) Explore pt's ICE
3) Explore and address pt's complaints specific to his condition
4) Explore pt's drug compliance
5) Explore any drug side effects
     -minor side effects: reassure, provide symptomatic relieve and encourage pt to continue treatment
                                  if still not relieved, withraw the tx
     -major side effects: ask specifically about drug toxicity
6) Reinforce pt's knowledge on TB and TB Tx
7) Safety Netting
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The Respi Clinic

65 years old chinese gentleman turned up at the Respi clinic as he developed generalised itchy maculopapular rashes on D8 of the treatment. He was then admitted for reintroduction of anti TB following the onset of adverse reactions on Akurit 4 + pyrodixine.
TB clinic check list:
1) Explore and address the pt's general complaints
2) Explore and address pt's complaints specific to his condition
3) Explore pt's ICE
4) Explore pt's drug compliance
5) Explore any drug side effects
     -minor side effects: reassure, provide symptomatic relieve and encourage pt to continue treatment
                                  if still not relieved, withraw the tx
     - Rifampicin (R)
        Isoniazid (H)
       Pyrazinamide (Z)
       Ethambutol (E)
       Streptomycin (S)       
     -major side effects: ask specifically about drug toxicity
     -double check on drug interactions:
       Rifampicin: Liver Enzyme Inducer - drug plasma level decrease secondary to increase drug metabolism
                                                             OHA, OCP, Oral anticoagulat (warfarin), Cyclsporin,    
                                                             Corticosteroids, Cimitedine, PI, Phenytoin, digitalis glycosides,
                                                            theophylline (Oral, Cs, Ps)
       Isoniazide: Liver Enzyme Inhibitor - drug plasma level increased secondary to decrease drug metabolism
                                                              Phenytoin, CBZ
6) Reinforce pt's knowledge on TB and TB Tx
     -dietry
     -excercise
     - herbal medicine
7) Safety Netting

59 years old obese lady referred to respi clinic TRO OHS (Obesity hypoventilation syndrome) with overlapping OSA. She has the following problems:
1) DM/ HPT
2) Decompensated CCF
3) TRO OHS with overlapping OSA
4) TRO COAD/ adult onset BA: previously working in a painting factory dealing with chemicals for many years and was involved in spraying chemical compounds. She developed sx of SOB with wheezing after stopped working 5 years ago which has become more frequent since the past 2 years. No positive FHx of BA, and there was no obvious PEFR reversibilty seen in the ward.

Investigations done:
HRCT: no evidence of intistial fibrosis
Lung function test: severe restriction
ECHO: poor window dt very obese pt, Mild MR and Mild TR, EF: 56%
ECG: poor R wave progression
ABG: Respiratory acidosis with Type 2 RF (ph 7.318  pco2 59  po2  47  hco3  25.4

Medications:
MDI combivent 2 puffs TDS
MDI seretide 2 puffs BD
montelukast 10mg ON
perindopril 4mg OD
metformin 1g BD
frusemide 40mg OD
aspirin 150mg OD
SR neulin 250mg OD
atorvastatin 40mg OD
Bromohexine 8mg TDS
SC actrapid 16u TDS
SC insulatard 26u ON

Chest clinic checklist:
1) Explore and address the pt's general complaints
2) Explore pt's ICE
3) Explore and address pt's complaints specific to his condition
    ESS
    Mallampati score
4) Explore pt's drug compliance
5) Explore any drug side effects
6) Reinforce pt's knowledge on her condition and current treatment
     -dietry
     -excercise
     - herbal medicine
7) Safety Netting
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Saturday 8 October 2011

NADI 2011

THE INCRETIN STORY -Evolving From Science to Clinical Practice

DIABETES AND RAMADHAN - Balancing glycemic control during Ramadhan

HYPOGLYCEMIA

DIABETES IN CKD















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Thursday 28 July 2011

ABG SAVES LIVES

http://orlandohealth.com/MediaBank/Docs/SLP/2010%20ABG%20SLP.pdf

The Normal Values:
  • pH: 7.35 - 7.45
  • pCO2: 35 - 45mmHg/ 4 - 6
  • pO2: 80 - 100mmHg/ 10 - 13
  • HCO3: 22 - 26mmHg
  • BE: +/- 3mEQ
Cellular Metabolism

HCO3-  +  H+  -->  CO2  +  H2O

  • The by-product of cellular mechanism is CO2 and H2O
  • CO2 is carried from the blood to the lungs
  • Excess CO2 will combine with H2O to produce H2CO3 (Carbonic Acid)
  • Why is it important to maintain normal cellular metabolism?
  • The shift of equation in to maintain the normal body pH:
    • CO2 will change the pH in the opposite direction (CO2 increase, PH decrease)
    • HCO3- will change the pH in the same direction (HCO3- increase, pH increase)

Interpretation of ABG:
  • ABG provides information on the pt's:
    • Oxygenation status
    • Acid-base balance status

Acid-Base Balance
  • Normal PH range : 7.35 - 7.45
  • This narrow normal PH range need to be maintain for normal cellular metabolism to take place
  • pH less than 6.8 and more than 7.8 is not compatible with life
  • Two main organs that are involved in the acid-base balance are the kidneys and the lungs
  • The body maintains the normal PH range by two buffering mechanisms/ systems:
    • Lung/ Respiratory buffer response (Respiratory Compensation)
    • Renal/ Metabolic buffer response (Metabolic Compensation)
Respiratory (Lungs) Buffer Response
  • Respiratory compensation takes 1-3min
  • The level of carbonic acid will eitrher increase/ decrease the rate and depth of ventilation until appropriate CO2 level is re-established
  • How does the carbonic acid increase/ decrease the rate and depth of ventilation? What is the underlying mechanism?

Metabolic (Renal) Buffer Response
  • Metabolic compensation will take hours to days
  • In the effort to maintain normal pH in the blood, the kidney either excrete or retain HCO3-
  • When the pH rises, the kidney will compensate by excreting HCO3- in the urine
  • When the pH decreases, the kidney will compensate by retaining HCO3-
  • What is the role of haemodyalisis in acid-base balance?
Oxygenation status in ABG
  • The component of ABG used to evaluate the blood oxygenation is paO2
  • Why is the pO2 lower then the sO2 in certain circumstances? The answer lies behind the Oxyhaemoglobin Dissociation Curve.
  • Type I Respiratory Failure
  • Type 2 Respiratory Failure
Respiratory Acidosis
  • Low pH, High pCO2
  • Differential Dx
  • Management

Respiratory Alkalosis
  • High pH, Low pCO2
  • Differential Dx
  • Management

Metabolic Acidosis
  • Low pH, Low HCO3-
  • Differential Dx
  • Management

Metabolic Alkalosis
  • High pH, High HCO3-
  • Differential Dx
  • Management


Compensation
  • In the event of an acid-base imbalance, the body attempts to compensate via two primary buffering response system which is the lungs and the kidneys
  • The aim is to restore the body normal pH for optimal cellular metabolism to take place
  • Compensation can be divided into:
    • Uncompensated
      • either the respiratory or metabolic component is abnormal, not both
      • pH is abnormal
    • Partially compensated
      • both the respiratory and metabolic components are abnormal
      • pH is abnormal
    • Fully compensated
      • both the respiratory and metabolic components are abnormal
      • pH is within the normal range
      • pH = 4 is the normal range
  • In compensation, we need to know:
    • are we dealing with acidosis or alkalosis
    • which system is the primary problem
    • which system is compensating

Mixed Respiratory and Metabolic Acidosis
  • Low pH
  • High pCO2 and Low HCO3-

Mixed Respiratory and Metabolic Alkalosis
  • High pH
  • Low pCO2 and High HCO3-

Chronic and Acute changes in ABG
  • Metabolic compensation takes hours to days
  • Respiratory compensation takes 1-3mins
  • Hence, a Full metabolic compensation indicates a chronic problem whereas a Full respiratory compensation indicates an acute problem

Other issues in ABG interpretation
    • What is the expected pco2 calculation in metabolic and respiratory acidosis?
    • What is the role of Anion Gap calculation in metabolic acidosis?
    • What is the role of Base excess calculation?
    • False results in ABG
    • Is it important to differentiate between a venous or arterial blood sample in ABG interpretation? How to differentiate between venous and arterial blood gases? How does this effect the ABG result interpretation? - regardless of whether it is venous or arterial, if pco2 is high - need to hyperventilate the patient, don't wait to repeat the ABG.


7.35 – 7.45

pH
7.29
ACIDOSIS
pCO2
30
ALKALOSIS
HCO3-
18
ACIDOSIS
PARTIALLY  COMPENSATED  METABOLIC  ACIDOSIS
pO2
80
LOW
pCO2
60
HIGH
TYPE 2  RESPIRATORY  FAILURE
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Wednesday 20 July 2011

CLINICAL PRACTICE GUIDELINES

MALAYSIA
1) Practical guide to Insulin Therapy in Type 2 Diabetes Mellitus
http://www.mems.my/file_dir/8744697374dc0e0db6586e.pdf
2) Academy of Medicine
http://www.acadmed.org.my/index.cfm?&menuid=67

WHO GUIDELINES

NICE GUIDELINES

References
1. http://www.mimsonline.com/mimsonline/
drugdetails.aspx?id=2398&dcname=My&SearchTy
pe=Brand
2. http://www.nlm.nih.gov/medlineplus/druginfo/
medmaster/a698009.html
3. http://www.medicinescomplete.com/mc/
martindale/current/17634-v.htm#m17634-a3-y
4. http://www.drugdigest.org/DD/DVH/Uses/
0,3915,352|Irbesartan,00.html#interactions
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CPG TYPE 2 DM Fourth Edition - 2009, CPG INSULIN THERAPY

Issues:
1) Hypoglycemia secondary to dilutional hypeglycemia
2) Tight Glycemic control in MI patients
3) Initiation of treatment in newly dx type 2 DM - OHA and Insulin
4) Insulin dose adjustment

A 50 years old gentleman presented to ED HSB with sudden onset of central chest discomfort radiated to the back, shoulder and left arm associated with sweating. pain relieved post Streptokinase

RF:
Smoker 15-20/ day for 30 years
HPT
Strong FHx
newly dx Type II DM

Background Hx:
HPT on T Atenolol 50mg BD
Staghorn calculus with renal impairment in 2008
Gout on NSAIDS

In the ward:
T lovastatin 20mg ON
T isordil 10mg TDS
T aspirin 150mg OD
T plavix 75mg OD
T carvidelol 3.125mg BD
Sc insulatard 10u ON
T metformin 500mg BD

Blood Ix: 18/7/2011
CK 317 (30-200)
LDH 467 (125-220)
AST 48 (5-34)

FBC: wcc 10.67 (4-11) hb 15.4 (13-17) plt 109 (110-450)
Lipid (mmol/l)
TG 14.06 (Lipaemic sample)
LDL 7.74
HDL 0.7
Tot Chol 14.84

HbA1c 11.9%

RP
Ur 6 (3.2 - 7.4)
Cr 144.9 (62 - 115)
Na 126 (136-145)
K 3 (3.5-5.1)

LFT
TP 67 (64 - 83)
Albumin/ Globulin ratio  0.76
Bili 14 (3.4 - 20.5)
ALT (42)
Albumin 29 (35-50)
ALP 80 (40-150)
Cl 92 (98-107)

RP 19/7/2011
Ur 5.9 (3.2 - 7.4)
Cr 154 (62 - 115)
Na 131 (136-145)
K 3.3 (3.5-5.1)
Cl 93

RP  21/7/2011
Ur 6.4 (3.2 - 7.4)
Cr 156 (62 - 115)
Na 131 (136-145)
K 3.3 (3.5-5.1)

Albumin 30
GGT 133.9 (5-85)
-------------
Baseline RP:
Feb 2009 ur 11.5  Cr 328  UA 695
(presented to uro with Left staghorn calculi)
RP within x1/52:  ur 7.5  Cr 155

CXR @20/7/2011
Mild cardiomegaly

ECHO @ 21/7/2011

ADJUSTING/ TITRATING INSULIN DOSE
http://www.mems.my/file_dir/8744697374dc0e0db6586e.pdf
Insulin Therapy - adjusting the dosage
http://www.fpnotebook.com/Endo/Pharm/InslnDsng.htm
http://tde.sagepub.com/content/32/1/19S.full
blood glucose conversion table
http://www.bcchildrens.ca/NR/rdonlyres/841862E6-5AE1-4938-A479-E6C38D615EA3/20417/glucoseunits.pdf
diabetes mx in ramadhan
http://www.medscape.com/viewarticle/412367
http://www.diabetes.org.my/article.php?aid=636
dm in children
http://www.rch.org.au/clinicalguide/cpg.cfm?doc_id=5189
pt information
http://www.uptodate.com/contents/patient-information-diabetes-mellitus-type-2-insulin-treatment
initiating treatment
http://care.diabetesjournals.org/content/32/1/193.full
practice guideline for type 2 dm
http://www.diabetes.org.my/file_dir/138985421945a7495312db5.pdf
titrating insulin
http://clinical.diabetesjournals.org/content/27/2/72.full
http://clinical.diabetesjournals.org/content/23/2/78.full
Dilutional effect of hyperglycemia
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CPG STEMI 2007 (Second Edition)


  • Cardiovascular deaths account for 20 - 25% of total death in govn hospital from 2000-2005
  • The high mortality is probably due to delay presentation, delay diagnosis resulting in delay treatment
  • Death most frequently occur soon after the onset of symptoms = Pre-hospital phase
  • Trials have shown that early reperfusion therapy results in myocardial salvage --> sig reduction in morbidity and mortality
  • Hence, need to educate the public regarding the sx and the need to present to hospital early
  • Also need to train the ED on the best way to deal with STEMI 
  • ACS=Unstable angina, STEMI, NSTEMI --> indicates ongoing myocardial ischemia
    • Unstable angina/ NSTEMI: Acute Subtotal occlusion of the coronary artery
    • STEMI: Acute Total occlusion of the coronary artery (Transmural)
  • ACS is most often caused by atherosclerotic occlusion of the coronary arteries (ruptured, fissured, ulcerated on top of thrombosis and coronary vasospasm)
  • Rarely, non artherosclerotic occlusion (coronary vasospasm alone, coronary embolism/ vasculitis) causes ACS
  • Typical chest pain --> ECG: no ST elevation --> cardiac biomarkers --> normal: Unstable angina
                                                                                                                          high : NSTEMI
                                     --> ECG: ST elevation --> STEMI
  • Criteria for STEMI:
  • ECG Changes:
    • Evolution of ECG changes (time frame - immediately post occlusion --> weeks --> moths --> years):
      • Hyperacute T waves/ Peaked T waves due to localized hyperkalemia
      • ST segment elevation at the J point - Concave appearance
      • ST segment elevation become more pronounced - change in morphology to convex, rounded upwards
      • ST segment elevation may become indistinguishable from T wave
      • Q wave develops (indicates irreversible myocardial death) with loss of R wave amplitude as the ST segment elevates
      • within x2/52 post MI:
        • ST segment returns to the isoelectric baseline
        • Deepen Q wave
        • T wave inversion
        • Reduced R wave amplitude
    • Pathophysiology of Myocardial Infarction:
      • Acute total occlusion of the coronary artery secondary to atherosclerotic or non atherosclerotic occlusion (rare) leads to myocardial necrosis   
      • Sequale of event post occlusion
    • Evolution of ECG changes in correlation with the cardiac biomarkers
    • The ECG leads effected depends on the location of infarct
      • Coronary artery anatomy
        • Left main stem and Right Coronary Artery arises from the ostia of the aortic valve
        • Left main stem divides into the Left Circumflex artery (LCX- supply) and the Left Anterior Descending Artery (LAD - supply the 2/3rd of the anterior interventricular septum and the anterior part of the heart)
        • RCA divides into the Posterior Descending Aretry (PDA - supply the psoterior interventricular septum). RCA supplies the SA node, AV node and Inferior border of the LV
      • ECG changes:
        • Inferior AMI
        • Anteroseptal AMI
        • Anterolateral AMI
        • Right sided Involvement
        • Posterior Involvement
    • Complications of Myocardial Infarction
    • Treatment of AMI:
      • Immediate
      • Post MI management: Physiorapist, cardiac rehab nurse referral 
      • Cardiac RF management:
        • BP control (how vigorous)
        • Blood gluscose control - Dietician referral
        • Hyperlipidaemia
      • Cardiac Rehabilitation
        • Advice to Post MI patients (The Do's and Dont's) 



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